Aula 4 - Cardiac Disease Flashcards
(214 cards)
1
Q
The blood always flows from _______ (higher/lower) pressure regions to _______ (higher/lower) pressure regions.
A
higher, lower
2
Q
How is the mean arterial pressure calculated?
A
Mean Arterial Pressure = Cardiac Output x Peripheral Vascular Resistance
3
Q
Changes in blood pressure are detected by _________ and corrected by _________.
A
the carotid and aortic sinus baroreceptors, the baroreflex and RAA system
4
Q
Which hormones are responsible for controlling the peripheral vascular resistance?
A
Atrial Natriuretic Peptide (ANP), Vasopressin, Epinephrin, Angiotensin II
5
Q
True or False: Both the sympathetic and parasympathetic nervous systems control the peripheral vascular resistance.
A
True
6
Q
The cardiac function is measured by the ________.
A
cardiac output
7
Q
What are the determinants of cardiac function?
A
Heart rate and stroke volume
8
Q
How is cardiac output calculated?
A
Cardiac Output (mL/min) = Heart Rate (/min) x Stroke Volume (mL)
9
Q
What are the determinants of the heart rate?
A
Electrical conduction system,sympathetic nervous system, and parasympathetic nervous system.
10
Q
What are the 5 main determinants of stroke volume?
A
Volemia, end diastolic volume, blood pressure, ventricular wall thickness, and contractility.
11
Q
What is the stroke volume?
A
Volume of blood pumped by the left ventricle during each systolic contraction.
12
Q
What is the baroreflex?
A
Homeostatic mechanism that helps to regulate blood pressure.
13
Q
The baroreflex is more sensitive to ___________ (increase/decrease) in blood pressure.
A
Decrease
14
Q
Where are the most sensitive baroreceptors located?
A
Carotid sinuses and aortic arch.
15
Q
What are baroreceptors?
A
Strech receptors (or mechanoreceptors) that sense blood pressure.
16
Q
What happens when the baroreflex detects a decresase in blood pressure?
A
Increase in heart rate + Increase in contractility of the left ventricle + Increase in peripheral vascular resistance
17
Q
What does RAAS stand for?
A
Renin-Angiotensin-Aldosterone System
18
Q
The aortic arch baroreceptors are predominantly responsive to ___________ (increases/decreases) in blood pressure.
A
Increases
19
Q
True or False: A decrease in blood pressure leads to the stretching of baroreceptors, triggering a depolarizing receptor potential.
A
False. An increase…
20
Q
A decrease of blood pressure leads to a decreased stretch of baroreceptors, triggering a __________ (depolarizing/hyperpolarizing) potential.
A
hyperpolarizing
21
Q
The baroreflex is a ________ (fast/slow) response to changes in blood pressure.
A
Fast
22
Q
The RAA system is a ________ (fast/slow) response to changes in blood pressure.
A
Slow
23
Q
Why is the baroreflex faster than the RAA system in responding to changes in blood pressure?
A
Because the baroreflex is a neural response, which is faster than the hormonal response of RAA.
24
Q
The RAA system regulates blood pressure by regulating ____________.
A
blood volume
25
Renin converts ___________ to _____________.
Angiotensinogen, angiotensin I
26
Angiotensin II causes the _____________ (vasodilation/vasoconstriction) of the arterioles, leading to ___________ (increased/decreased) peripheral vascular resistance.
vasoconstriction, increased
27
What is the first step of the RAA system?
Release of the enzyme Renin in the kidney in response to reduced perfusion pressure.
28
What enzyme is responsible for converting Angiotensin I to Angiotensin II? Where does this conversion happen?
Angiotensin Converting Enzyme (ACE). It happens mainly in the lung endothelium, but also happens in smaller quantities in the renal endothelium.
29
Angiotensin II ________ (increases/decreases) H2O and Na+ reabsorption.
Increases
30
What are the main 10 risk factors of cardiac disease?
1. Sex
2. Age
3. Familial hereditary traits
4. Tobacco use
5. Hypertension
6. Diabetes mellitus
7. Dyslipidemia (abnormal levels of lipids in the blood)
8. Obesity (IMC > 30kg/m2)
9. Stress
10. Inadequate lifestyles (sedentarism, sodium and hypercaloric-based diet, drug abuse)
31
What is a heart failure?
Decrease or loss of the heart's pumping ability.
32
What are the 7 general main causes of heart failure?
1. Ischemic heart disease
2. Hypertension
3. Medication
4. Arrhythmias
5. Cardiomyopathy
6. Pericardial disease
7. Endocardial disease
33
Can a chronic heart failure turn into an acute heart failure?
Yes, due to **decompensation** as a result of new medication or new disease.
34
What is the ejection fraction and how is it calculated?
The ejection fraction is the portion of blood present in the left ventricle at the end of the diastolic filling that is pumped by the left ventricle in the systolic contraction. It is calculated as:
EF (%) = Amount of blood **pumped out** / Amount of blood **in the chamber**
35
In systolic dysfunction, the ejection fraction is _________ (increased/normal/reduced).
Reduced
36
In diastolic dysfunction, the ejection fraction is ___________ (elevated/normal/reduced).
Normal
37
What are the 6 main general causes of systolic dysfunction?
1. Ischemic heart disease
2. Endocardial disease
3. Hypertension
4. Diabetes mellitus
5. Renal disease
6. Infiltrative disease
38
What are the main 3 specific causes of systolic dysfunction?
1. Arrythmias
2. Myocarditis
3. Dilated cardiomyopathy
39
What are the 3 main specific causes of diastolic dysfunction?
1. Pericardial disease
2. Hypertrophic cardiomyopathy
3. Restritive cardiomyopathy
40
What are two conditions that can lead to left heart failure due to volume overload?
Anemia and hyperthyroidism
41
What is one cause of left heart failure due to volume overload?
Valvular insufficiency
42
Name two causes of left heart failure related to pressure overload.
Hypertension and ejection obstruction
43
What is AV valvular stenosis, and how does it contribute to left heart failure?
It is the narrowing of the atrioventricular valve, reducing the filling of the left ventricle and leading to heart failure.
44
Besides AV valvular stenosis, name two other causes of left heart failure due to decreased filling.
Pericardial disease and infiltrative diseases
45
How does myocardial infarction lead to left heart failure?
It causes the loss of cardiomyocytes, reducing the heart’s ability to pump effectively.
46
What connective tissue diseases can contribute to left heart failure?
Diseases that cause fibrosis or inflammation of the myocardium, leading to loss of heart function.
47
How do infections contribute to decreased heart contractility and left heart failure?
They can cause myocarditis, leading to inflammation and weakening of the heart muscle.
48
What are the two main causes of decrease in heart contractility and, consequently, left heart failure?
Toxic substances (drugs, alcohol, etc.) and infections
49
What is systolic dysfunction in left heart failure?
A condition where end-diastolic volume (EDV) is greater than stroke volume (SV), leading to decreased cardiac output.
50
What are the 3 compensatory mechanisms that the heart uses to maintain cardiac output in systolic dysfunction?
* Frank-Starling mechanism
* Increase in catecholamines (↑HR, ↑SV)
* Myocardial hypertrophy (↑EDV ⇒ ↑SV)
| EDV - end-diastolic volume; SV - stroke volume
51
What happens when compensatory mechanisms in systolic dysfunction fail?
Heart failure persists, leading to reduced cardiac output and systemic complications.
52
What is diastolic dysfunction in left heart failure?
A condition where end-diastolic pressure increases due to impaired ventricular relaxation.
53
In diastolic dysfunction, there is a ____________ (decreased/increased) relaxation capability, ____________ (decreased/increased) elastic tension and ____________ (decreased/increased) ventricular rigidity.
Decreased, decreased, increased
54
Is contractility affected in diastolic dysfunction?
No, contractility is generally kept!
55
Left heart failure leads to ____________ (increased/decreased) cardiac output and ____________ (increased/decreased) blood pressure.
decreased, decreased
56
Why is there an increased Sympathetic Nervous System (SNS) activity after heart failure?
It's a compensatory mechanism in which the body tries to increase heart rate and contractility to compensate for low cardiac output.
57
How does heart failure affect cardiac output and blood pressure?
It decreases cardiac output (↓CO) and decreases blood pressure (↓BP).
58
What is the role of the sympathetic nervous system (SNS) in left heart failure?
The sympathetic NS is activated to compensate for reduced cardiac output, leading to vasoconstriction and increased afterload.
59
How does left heart failure affect the renal system?
It increases renin-angiotensin-aldosterone (RAA) system activation and increases vasopressin, which contribute to fluid retention and vasoconstriction.
60
What inflammatory mediators are increased in heart failure?
Cytokines such as interleukins (ILs) and tumor necrosis factor-alpha (TNFα), as well as endothelins.
61
How does heart failure contribute to structural heart changes?
It leads to cardiomyocyte hypertrophy (enlargement of heart muscle cells) and increased vasoconstriction.
62
What hemodynamic effects are seen in left heart failure?
Increased afterload and increased blood pressure due to compensatory mechanisms.
63
The activation of the sympathetic nervous system in heart failure leads to ________________, which is the narrowing of veins, and to ________________, which is the narrowing of arteries.
venoconstriction, vasoconstriction
64
Venoconstriction increases ____________ (preload/afterload) and vasoconstriction increases ____________ (preload/afterload).
preload, afterload
65
What is preload and afterload?
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. In other words, preload is the amount of blood filling the heart
Afterload is the force or load against which the heart has to contract to eject the blood. In other words, afterload is the resistance the heart has to pump against.
66
In left heart failure, the kidneys sense a ________ (high/low) blood pressure and activate the RAA system.
low
67
What are the two main neuro-endocrine systems activated in response to low blood pressure in heart failure?
Sympathetic Nervous System (SNS) and Renin-Angiotensin-Aldosterone System (RAAS)
68
What are the effects of increased Sympathetic Nervous System (SNS) activity in heart failure?
Venoconstriction (increased preload) and Vasoconstriction (increased afterload)
69
What are the effects of the Renin-Angiotensin-Aldosterone System (RAAS) activation in heart failure?
Increased Glomerular Filtration Rate (GFR) and Increased Vasopressin (ADH), which both lead to fluid retention.
70
What is the result of the compensatory mechanisms in early heart failure on preload and afterload?
Increased preload and Increased afterload
71
What inflammatory mediators are increased in chronic heart failure?
Cytokines (ILs, TNFα) and Endothelins
72
What is the result of persistent neuro-endocrine activation on blood pressure in chronic heart failure?
Increased blood pressure
73
True or False: Left heart failure triggers neuro-endocrine responses to maintain blood pressure and cardiac output.
True
74
True or False: The neuro-endocrine responses to left heart failure lead to decreased preload and afterload, worsening heart failure.
False.
The neuro-endrocrine responses **increase preload and afterload**, worsening heart failure.
75
In left heart failure, ____________ (increased/decreased) resistance in the systemic circulation leads to left ventricular insufficiency, which causes congestion in the pulmonary circulation.
increased
76
In left heart failure, there is ________ (resistance/congestion) in the systemic circulation and ________ (resistance/congestion) in the pulmonary circulation.
resistance, congestion
77
True or False: Left ventricular insufficiency leads to congestion in pulmonary circulation.
True.
Left ventricular insufficiency is the inability of the left ventricle to pump blood effectively, which leads to congestion, i.e. buildup of blood, in the pulmonary circulation.
78
What are the 7 main clinical manifestations of left heart failure?
* Dyspnea (shortness of breath)
* Nocturnal paraoxystic dyspnea (sensation of shortness of breath that awakens the patient)
* Ortopnea (difficulty breathing when lying down)
* Cardiac asthma (a type of coughing or wheezing that occurs with left heart failure)
* Fatigue and mental confusion
* Nocturia (the need for patients to get up at night regularly to urinate)
* Thoracic pain
79
True or False: Cardiogenic pulmonary edema is one of the main complications of left heart failure.
True.
Cardiogenic pulmonary edema is mainly caused by left ventricular failure and it is a life-threatening collection of too much fluid in the lungs.
80
Can left heart failure lead to right heart failure?
Yes, in fact it is one of the main causes.
81
What is Cor Pulmonale?
Cor Pulmonale is an enlarged right ventricle of the heart, caused by a primary disorder of the respiratory system, and it may cause right heart failure.
82
What are the 3 primary causes of Cor Pulmonale?
* **Hypoxia-induced vasoconstriction:** pulmonary vascular resistance rapidly increases as oxygen tension decreases.
* **Pulmonary embolism:** it's a blood clot that develops in a blood vessel elsewhere in the body (often the leg), travels to an artery in the lung, and suddenly forms a blockage of the artery.
* **COPD (Chronic Obstructive Pulmonary Disease):** happens when the lungs become inflamed, damaged and narrowed.
83
What congenital conditions can cause Pre-capillary Obstruction?
Congenital shunts or obstructions.
84
What cardiac event can lead to Cardiomyocyte Loss (loss of heart muscle cells in the right ventricle) in the right ventricle?
Acute myocardial infarction (right ventricle)
85
What are the four main categories of causes for right Heart Failure?
* Left Heart Failure
* Cor Pulmonale
* Pre-capillary Obstruction
* Cardiomyocyte Loss
86
What is a cause of Pre-capillary Obstruction characterized by high blood pressure in the pulmonary arteries?
Idiopathic pulmonary hypertension
87
In right heart failure, ____________ (increased/decreased) resistance in the pulmonary circulation leads to right ventricular insufficiency, which causes congestion in the systemic circulation.
increased
88
In left heart failure, there is a ________ congestion, while in right heart failure there is a ________ congestion.
pulmonary, systemic
89
Pulmonary disease (e.g. Cor Pulmonale) is a common cause of ________ (left/right) heart failure.
right
90
In left heart failure, there is a ________ (aortic/pulmonary) valve stenosis, while in right heart failure there is a ________ (aortic/pulmonary) valve stenosis.
aortic, pulmonary
91
What are the main clinical manifestations of right heart failure?
* Systemic venous congestion
* Dyspnea
92
What is a visible sign of systemic venous congestion in the neck?
Jugular venous distention (or jugular venous turgescence)
93
What occurs in the splanchnic territory due to hepatic congestion in Right Heart Failure?
Hepatojugular reflux, ascites, abdominal pain
94
What is the term for generalized severe edema involving multiple venous territories?
Anasarca
95
What previous condition can cause dyspnea in Right Heart Failure?
Previous Left Heart Failure (leading to pulmonary edema)
96
What is ischemic heart disease?
Heart damage caused by narrowed heart arteries, which result in poor blood and oxygen supply to the heart.
97
What is the most frequent cause of ischemic heart disease?
Atherosclerosis (buildup of fats, cholesterol and other substances in and on the artery walls).
98
What are some factors that can trigger vasospasm in coronary arteries?
Histamine, serotonin, catecholamines, endothelial factors, and medications.
99
Does vasospasm-induced ischemic heart disease have a relation to exertion?
No
100
What is a potential source of emboli that can cause ischemic heart disease?
Endocarditis vegetations (growths on heart valves).
101
What is the primary congenital cause of ischemic heart disease?
Coronary abnormalities.
102
What are the 4 main general causes of ischemic heart disease?
1. **Atherosclerosis** (buildup of fats, cholesterol and other substances in and on the artery walls).
2. **Vasospasm** (a condition in which an arterial spasm leads to vasoconstriction).
3. **Embolism** (an obstruction or blockage in a blood vessel).
4. **Congenital ischemic heart disease** (birth defects that affect the normal way the heart works).
103
True or False: Atherosclerosis, as a cause of ischemic heart disease, is not related to exertion.
False.
Atherosclerosis is often related to exertion (physical activity).
104
Ischemia occurs with ____ % occlusion while resting and ____ % occlusion during exertion.
90, 50
105
Ischemia pathophysiology can originate due to ________ (increased/decreased) O2 consumption and/or ________ (increased/decreased) O2 delivery.
increased, decreased
106
What are the 3 main causes of an increased O2 consumption, that might lead to ischemia?
* **Thyrotoxicosis**: occurs when there are abnormally high blood levels of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), which increase metabolic rate (i.e., increase the heart's oxygen demand).
* **Aortic stenosis**: narrowing of the aortic valve opening, which causes an increased workload that leads to left ventricular hypertrophy (thickening of the heart muscle) and this enlarged muscle requires more oxygen.
* **Medication**
107
What are the 3 main causes of an decreased O2 delivery, that might lead to ischemia?
* **Coronary obstruction**: a thrombus (blood clot) can obstruct or completely block an artery, leading to severe ischemia or infarction.
* **Carbon Monoxide (CO) poisoning**: CO binds to hemoglobin in red blood cells much more strongly than oxygen. This reduces the oxygen-carrying capacity of the blood, leading to tissue hypoxia (oxygen deficiency).
* **Medication**
108
How can rupture of plaque lead to ischemia?
**Plaque rupture** happens when the fibrous cap that covers the plaque breaks open. With plaque erosion, the fibrous cap stays intact, but endothelial cells around the plaque get worn away, causing **endothelial dysfunction**. Both events lead to the formation of a blood clot, due to **platelet aggregation**, and to the **release of autacoids** (local hormones produced in tissues), such as thromboxane A2 and serotonin. All of this leads to a **decrease in perfusion** (aka ischemia).
109
What are the autacoids (local hormones) released after plaque rupture, during platelet aggregation?
**Thromboxane A2** (potent platelet activator and vasoconstrictor, produced by activated platelets during hemostasis) and** serotonin** (released by platelets to narrow arterioles, slowing blood flow and helping to form clots).
110
Rupture of plaque leads to a ____________ (decrease/increase) in perfusion, resulting in ischemia.
decrease
111
What happens to PO2 levels due to decreased perfusion?
Decreased perfusion leads to a decrease in the partial pressure of oxygen (PO2) in cells.
112
What metabolic process occurs in cells due to decreased PO2?
The lack of oxygen leads to anaerobiosis (lactic acid production) and glycogen depletion.
113
What is the direct result of the changes in cellular metabolism due to decreased perfusion?
Cellular lesion
114
What is the clinical manifestation of cellular lesion in ischemic heart disease?
Angina pectoris (chest pain)
115
What are the 4 main changes in cellular metabolism due to reduced perfusion in ischemia?
1. Decrease in PO2
2. Anaerobiosis (lactic acid) and glycogen depletion
3. Mitochondrial “edema” and membrane lesion (cellular lesion)
4. Dysfuncion of contraction-relaxation cycle
116
True or False: Angina pectoris is an early manifestation of ischemia.
False.
Angina pectoris is considered a "late" manifestation of angina (after 30s).
117
True or False: Angina pectoris aggravates with respiration.
False.
Angina pectoris does not aggravate with respiration.
118
What is the evolution of angina pectoris?
First, it is a stable angina (pain only in exertion). Then it becomes unstable (pain while resting as well). And finally it presents as an acute myocardial infarctation, where the pain is uninterrupted for over 10 minutes.
119
True or False: Most patients with myocardial infarctation are assymptomatic.
True.
Myocardial infarctation is assymptomatic in 80% of patients.
120
Why are most myocardial infarctation patients assymptomatic?
1. Transient perfusion decrease (that resolves).
2. Afferent nervous dysfunction (for example, due to cardiac transplantation or diabetes mellitus, which make them feel less pain).
3. Different thresholds of pain.
121
What are the main 4 clinical manifestations of angina pectoris?
1. S4 and dispnea: systolic and diastolic dysfunction.
2. Nausea and voming: activation of the vagus nerve.
3. Tachycardia (fast heart rate): increased catecholamine levels.
4. Bradycardia (slow heart rate): lesion of the AV node (infarction by occlusion of the right coronary artery) and activation of the vagus nerve.
## Footnote
NOTE: Catecholamines increase heart rate, blood pressure, breathing rate.
122
What gastrointestinal symptoms can occur in angina pectoris or myocardial infarction?
Nausea and vomiting
123
What nerve activation is associated with nausea and vomiting in angina pectoris/myocardial infarction?
Activation of the vagus nerve
124
What cardiac manifestation can occur due to a lesion of the AV node in myocardial infarction?
Bradycardia (slow heart rate)
125
What are the main complications of acute myocardial infarctation?
* Cardiogenic shock (hypotension due to severe HF)
* Arrhythmias
* Thrombosis
126
What happens when acute myocardial infarction causes occlusion of the descending left coronary artery?
There is a rupture of the ventricular septum, allowing **interventricular communication**.
127
What complication happens when acute myocardial infarction causes occlusion of the left anterior descending coronary artery and the circumflex artery?
Cardiac tamponade
128
Arrythmias may cause ventricular fibrillation, which ________ (lowers/increases) cardiac output and leads to acute myocardiac infarctation.
lowers
129
Why is thrombosis a complication of acute myocardial infarctation?
Because there is activation of the factors of hemostasis by the damaged myocardium, which lead to venous stasis and thrombosis.
130
What are the 4 valves of the heart?
* Aortic
* Pulmonary
* Mitral
* Tricuspid
131
What are the two main categories of valve disease?
* Valve stenosis (valves can't open properly)
* Valve insufficiency (valves can't close properly)
132
Order the following steps:
* Pulmonary hypertension
* Aortic stenosis
* Obstruction of ejection in the left ventricle
* Systolic dysfunction
* Left ventricular hypertrophy
* Left heart failure
* Right heart failure
1. **Aortic stenosis** (narrowing of the aortic valve, which connects the LV to the aorta)
2. **Obstruction of ejection in the LV** (the narrowed valve will restrict the blood flow out of the LV to the aorta)
3. **Left ventricular hypertrophy** (compensatory response to the increased pressure in the LV, where there is a thickening and enlargement of heart muscle in the LV walls).
4. **Systolic dysfunction** (the heart becomes inable to meet its demand and generate sufficient arterial blood pressure and cardiac output)
5. **Left heart failure** (the left ventricle is gradually weakened and loses its ability to pump blood to the systemic circulation)
6. **Pulmonary hypertension** (abnormally high blood pressure in the pulmonary circulation, due to narrowing of the arteries, which demands an even higher pressure in the right ventricle to be able to pump the blood to the pulmonary arterie)
7. **Right heart failure** (the right ventricle is unable to pump enough blood to the pulmonary circulation)
133
What is aortic stenosis?
Narrowing of the aortic valve opening (between the left ventricle and the aorta) that restricts blood flow from the left ventricle to the aorta.
134
What is aortic insufficiency?
Regurgitation (backflow) of the blood from the aorta into the left ventricle, when the aortic valve can't close properly.
135
What are the compensatory mechanisms for acute regurgitation?
None
136
What are the compensatory mechanisms for chronic regurgitation (e.g. in aortic insufficiency)?
Long QT interval
## Footnote
The QT interval is the time from the beginning of the QRS complex, representing ventricular depolarization, to the end of the T wave, resulting from ventricular repolarization.
137
What are the 3 main manifestations of left heart failure due to aortic insufficiency?
* Dyspnea (cardiogenic pulmonary oedema)
* Arterial hypotension
* Hyperdynamic pulses
138
True or False: A prolonged QT interval is a marker of advanced aortic insufficiency.
True.
A long QT interval is a compensatory mechanism of chronic aortic insufficiency.
139
What is mitral stenosis?
Narrowing or blockage of the mitral valve, which is located between the left atrium and the left ventricle.
140
What are 4 main types of mitral stenosis?
* **Rheumatic mitral stenosis** (narrowing og the mitral valve as a consequence of rheumatic fever, an autoimmune inflammatory process that causes inflammation in many organs, including the heart)
* **Dystrophic calcification** (which causes mitral stenosis): dystrophic calcium deposition to the mitral valve.
* **Congenital heart malformation** (abnormal morphology of the mitral valve)
* **Tumoral mitral stenosis** (narrowing of the mitral valve due to a tumor)
141
Order the following steps:
* Pulmonary hypertension
* Dilation of the left atrium
* Mitral stenosis
* Right heart failure
* Obstruction of the filling of the left ventricle
1. **Mitral stenosis** (narrowing of the mitral valve, restricting the blood flow from the left atrium to the left ventricle)
2. **Obstruction of the filling of the left ventricle**
3. **Dilation of the left atrium** (enlargement of the left atrium due to pressure or volume overload)
4. **Pulmonary hypertension** (the dilation of the left atrium compressses the pulmonary artery, causing an increased blood pressure)
5. **Right heart failure** (the right ventricle is not able to pump blood to the pulmonary circulationdue to the high blood pressure in the pulmonary artery)
142
Mitral stenosis leads to ____________ (increased/decreased) ventricular diastolic filling, ____________ (increased/decreased) cardiac output and ____________ (increased/decreased) distal perfusion (i.e. organ and tissue perfusion).
**decreased** (the blood cannot pass from the left atrium to the left ventricle)
**decreased** (since there is less blood in the left ventricle, less blood is pumped out of the heart)
**decreased** (less blood pumped out of the heart means less blood reaching organs and tissues)
143
What are the 3 main clinical manifestations of mitral stenosis?
* Pulmonary edema (dyspnea, ortopnea, nocturnal paraoxystic dyspnea)
* Fatigue
* Palpitations (arrhythmia)
144
What are the 3 main cardiomyopathies?
* Dilated cardiomyopathy
* Hypertrophic cardiomyopathy
* Restrictive cardiomyopathy
145
What are cardiomyopathies?
Diseases of the myocardium (heart muscle).
146
What are the 6 clinical manifestations of dilated cardiomyopathy?
* Dyspnea (shortness of breath) during exertion
* Angina pectoris (chest pain)
* Palpitations
* Abdominal and peripheral edema (inflammation)
* Jugular venous turgor (visually enlarged jugular vein)
* Bilateral pulmonary rales or crackles (abnormal lung sounds heard during auscultation, described as crackling or bubbling sounds)
147
What are the 3 clinical manifestations of hypertrophic cardiomyopathy?
* Dyspena
* Dizziness
* Fainting
148
What are the 4 clinical manifestations of restrictive cardiomyopathy?
* Dyspnea
* Right heart failure symptoms
* Kussmaul sign (an increase in the jugular venous pulse when the patient inhales)
* Fourth heart sound (S4) (an abnormal heart sound)
149
What is the Frank-Starling mechanism?
The Frank-Starling mechanism is a physiological principle that explains how the heart responds to changes in venous return. Increases in venous return cause the heart's chambers to fill with more blood, which then causes the heart to stretch and contract more forcefully, and pump more blood out to the rest of the body.
150
What is the principle of Starling's law?
It states that the force of ventricular contraction is increased when the ventricle is stretched prior to contraction.
151
Order the following steps in dilated cardiomyopathy:
* Systolic dysfunction
* Frank-Starling mechanism
* Eccenctric hypertrophy and left ventrical dilation
* Cardiotoxic factors
1. Cardiotoxic factors (factors that damage the heart's muscle or lead to eletrophysiology dysfunction)
2. Frank-Starling mechanism
3. Eccentric hypertrophy and left ventrical dilation
4. Systolic dysfunction
152
Cardiac lesion leads to ____________ (increased/decreased) contractility, triggering the Frank-Starling mechanism.
decreased
153
In dilated cardiomyopathy, the increased ventricular diastolic filling (VDF) leads to ____________ and ____________.
1. **Eccentric hypertrophy** (characterized by increasing myocyte length, which ultimately results in a dilated left ventricle with thin walls)
2. **Left ventricle dilation**
154
Dilated cardiomyopathy is caracterized by ____________ (increased/decreased) contractility.
decreased
155
What is dilated cardiomyopathy?
It's a type of myocardium (heart muscle) disease that causes the heart chambers (ventricles) to thin and stretch, growing larger and becoming unable to pump blood by losing its contractility.
156
What is hypertrophic cardiomyopathy?
It's a type of myocardium (heart muscle) disease that causes the thickening of the heart muscle, compromising the ventricular diastolic filling due to lower ventricular volume.
157
In dilated cardiomyopathy, the walls of the ventricles become ________ (thinner/thicker) due to an ____________ (eccentric/concentric) hypertrophy.
thinner, eccentric
158
In hypertrophic cardiomyopathy, the walls of the ventricles become ________ (thinner/thicker) due to an ____________ (eccentric/concentric) hypertrophy.
thicker, concentric
159
Order the following steps in hypertrophic cardiomyopathy:
* Mitral insufficiency
* Concentric hypertrophy
* Cardiotoxic factors
* Hypertrophy of the interventricular septum
1. Cardiotoxic factors (factors that damage the heart's muscle or lead to eletrophysiology dysfunction)
2. Hypertrophy of the Interventricular septum (wall that separates the two ventricles)
3. Concentric hypertrophy (abnormal increase in left ventricular myocardial mass caused by chronically increased workload on the heart)
4. Mitral insufficiency
160
True or False: In hypertrophic cardiomyopathy, the left ventricle wall becomes thicker than the interventricular septum.
**False.**
The hypertrophy in the interventricular septum is larger than the hypertrophy of the left ventricle. Harmful factors damage the heart, causing the wall between the ventricles to thicken more than the left ventricle's main wall.
161
Hypertrophic cardiomyopathy is caracterized by ____________ (increased/decreased) obstruction to ejection.
increased
162
In hypertrophic cardiomyopathy, an increased obstruction to ejection leads to ________ (concentric/eccentric) hypertrophy, which ________ (increases/decreases) the volume of the left ventricle, further increasing obstruction to ejection.
* **concentric** (thickening of the left ventricle walls)
* **decreases** (the walls become thicker, resulting in less chamber volume)
163
What is restrictive cardiomyopathy?
It's a myocardium disease in which the muscle tissue in the ventricles becomes stiff, restricting the filling of the ventricles and leading to reduced blood flow in the heart.
164
What causes the increased stiffness of the myocardium in restrictive cardiomyopathy?
Connective tissue proliferation
165
What is compliance?
The term compliance is used to describe how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood. Physically, compliance (C) is defined as the change in volume (ΔV) divided by the change in pressure (ΔP).
166
In restrictive cardiomyopathy, elasticity is ________ (increased/decreased) and compliance is ________ (increased/decreased).
decreased (the muscle tissue becomes stiff), decreased (the muscle tisse can't expand properly)
167
What happens to the atriums in restrictive cardiomyopathy?
The atriums become dilated due to loss of elasticity and compliance.
168
What is the main consequence of restrictive cardiomyopathy?
Systemic venous congestion
169
In restrictive cardiomyopathy, the volume of the ventricles ____________ (increases/decreases) and the volume of the atriums ____________ (increases/decreases).
decreases, increases
170
True or False: In restrictive cardiomyopathy, the ventricles walls become thicker, which reduces the volume of the ventricles.
True
171
In hypertrophic cardiomyopathy, why does concentric hypertrophy lead to mitral insufficiency?
The narrowing caused by hypertrophy and increased velocity of blood flow through the obstructed area can lead to mitral regurgitation (blood leaking back through the mitral valve) **due to the Venturi effect** (a decrease in pressure in areas of high flow velocity).
172
What is the Venturi effect?
The Venturi effect describes how the velocity of a fluid increases as the cross section of the container it flows in decreases.
173
True or False: In restrictive cardiomyopathy, the ejection fraction is normal or decreased.
False.
In restrictive cardiomyopathy, the ejection fraction is normal or **increased**.
174
What is pericardial disease?
It's an **inflammatory** process involving the pericardium, a fibrous, double-walled and fluid-filled sac that surrounds the heart and great vessels.
175
An acute pericardial disease is called ________, which can evolve to chronical pericardial disease called ____________.
Pericarditis, Pericardial effusion
## Footnote
Pericardial effusion = derrame pericárdico
176
What are the main 4 causes of pericardial disease?
* Infection
* Trauma
* Acute myocardial infarctation
* Connective tissue disorder
177
What is Pericarditis?
Pericarditis is an inflammation of the pericardium.
178
What is Pericardial effusion?
A pericardial effusion is an abnormal accumulation of fluid in the pericardial cavity.
179
In pericarditis, calcium deposition occurs in the ________ (acute/chronic) inflammatory phase, while fibrin deposition occurs in the ________ (acute/chronic) inflammatory phase.
chronic, acute
180
Why is the heart filling compromised by chronic pericarditis (pericardial effusion)?
The accumulation of fluid in the pericardial cavity constricts the heart due to buildup of pressure, compromising the heart's ability to fill up with blood.
181
True or False: In chronic pericarditis, there is fibrous cicatrization of the pericardium.
True
182
What are 3 main clinical manifestations of (acute) pericarditis?
* Intermittent fever
* Pleuritic pain (sharp chest pain that worsens during breathing)
* Pericardial friction rub sound in auscultation (resembles the sound of squeaky leather)
183
What are the pulmonary clinical manifestations of pericardial effusion?
Dyspnea and fatigue (pulmonary edema)
184
What are the hepatic clinical manifestations of pericardial effusion?
Hepatomegaly and hepatojugular reflux (hepatic venous congestion)
185
What is the main consequence of pericardial effusion?
The heart filling is compromised, reducing cardiac output and leading to pulmonary and systemic circulation congestion due to regurgitation.
186
What are the 5 main manifestations of systemic and pulmonary congestion in pericardial effusion?
1. Dyspnea
2. Fatigue
3. Kussmaul's sign
4. Hepatomegaly
5. Hepatojugular reflex
187
What is the Kussmaul's sign?
It's an increased jugular venous pressure with inspiration, which leads to a visible jugular venous distention.
188
Besides the manifestations of systemic and pulmonary congestion, what are the other two main manifestations of pericardial effusion?
* **Paradoxical Pulse** (abnormal decrease in pulse wave amplitude during inspiration)
* **Pericardial Knock** (a high-pitched sound made by the heart due to early diastole, as a ventricle does not fully fill with blood between heartbeats)
189
What is arrhythmia?
Abnormal or irregular heartbeat
190
Distinguish the two main types of arthythmia.
* **Bradyarrhythmia** (Sinus bradycardia): slower-than-typical heart rate (< 60 bpm).
* **Tachyarrhythmia** (Sinus tachycardia): faster-than-typical heart rate (> 100 bpm).
191
What is the sick sinus syndrome?
## Footnote
Sick sinus syndrome = Síndrome do nódulo sinusal
Alternating bradycardia and tachycardia
192
What is an atrioventricular block?
It's a heart rhythm disorder that causes alterations in the atrioventricular electrical conduction, which becomes slower or blocked.
193
How many degrees of block are there in atrioventricular block?
Three
194
What is fibrillation?
Rapid, erratic heartbeats (uncoordinated series of very rapid, ineffective contractions of the ventricles) that cause the heart to abruptly stop pumping blood.
195
Is age a risk factor of atrial fibrillation?
Yes, it is more common in old age
196
What causes atrial fibrillation?
Irregular electrical activity with multiple sites of auricular depolarisation.
197
In atrial fibrillation, the P-wave is ________ (normal/prolonged/shortened/absent) and the QRS complexes are ________ (normal/irregular/absent).
absent, irregular
198
Why is there a risk of thromboembolism in atrial fibrillation?
The irregular electrical activity in the heart leads to inneficient auricular contraction, which causes blood to stagnate within the atriums and stagant blood is more prone to clotting, increasing the risk of forming a thrombi.
199
What causes ventricular fibrillation?
Irregular electrical activity with multiple sites of ventricular depolarisation.
200
In ventricular fibrillation, the P-wave is ________ (normal/prolonged/shortened/absent) and the QRS complexes are ________ (normal/irregular/absent).
absent, absent
201
What is more serious: atrial or ventricular fibrillation? Why?
Ventricular fibrillation, as it may lead to cardiac arrest and death.
202
What is shock?
Rapid decrease in arterial blood pressure, with reduced blood flow to the organs, leading to their dysfunction.
203
What are the 3 main types of shock?
1. Hypovolemic Shock
2. Distributive Shock
3. Cardiogenic Shock
204
Hypovolemic Shock is caused by a decrease in ________.
blood volume (volemia)
205
Distributive Shock is caused by a decrease in ________.
vascular resistance
206
Cardiogenic Shock is caused by a decrease in ________.
cardiac output
207
What causes the decreased vascular resistance in Distributive Shock?
Systemic vasodilation and capillary drainage
208
What are the consequences of Cardiogenic Shock?
It's characterized by **low blood pressure** (systolic below 90 mmHg), **decreased cardiac output**, and **reduced urine output (oliguria)**, indicating that the kidneys are not receiving enough blood flow.
209
What are the 3 main causes of Distributive Shock?
Distributive shock occurs when there's widespread vasodilation (widening of blood vessels) and/or capillary leak, leading to a relative decrease in blood volume. This can be caused by:
* **Septic shock**: Due to severe infection.
* **Neurogenic shock**: Due to damage to the nervous system.
* **Anaphylactic shock**: Due to a severe allergic reaction.
210
Connect each uppercase letter with the respetive lowercase letter:
A. Cardiogenic shock
B. Hypovolemic shock
C. Distributive shock
a. Volume-related
b. Blood vessel-related
c. Heart-related
A. c
B. a
C. b
211
In shock, a ________ (high/low) blood pressure leads to ________ (high/low) levels of oxygen in the blood, causing organ damage.
low, low
212
What are the 3 main complications of shock?
* **Acute Renal Failure/Acute Kidney Injury**
* **Disseminated Intravascular Coagulation (DIC)**: abnormal blood clotting throughout the body's blood vessels.
* **Acute Respiratory Distress Syndrome (ARDS)**: lung failure due to fluid buildup in your lungs and low blood oxygen levels.
213
In shock, metabolism and body temperature are ________ (increased/decreased).
decreased
| (due to low oxygen)
214
What are the risks of untreated Pericarditis?
* Pericardial effusion → Cardiac tamponade (life-threatening compression of the heart).
* Recurrent pericarditis (especially in autoimmune causes).
* Constrictive pericarditis (fibrosis leading to heart failure).
